Yuping Wang1, Qin Dong1, Yang Gu1, Lynn J Groome1. 1. Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center - Shreveport, Shreveport, LA, USA.
Abstract
PROBLEM: To determine whether miR-203 mediates endothelial inflammatory response in preeclampsia. METHOD OF STUDY: Maternal vessel miR-203 expression was assessed by in situ hybridization. Suppressor of cytokine signaling-3 (SOCS-3) and ICAM expression was determined by immunostaining. Subcutaneous fat tissue sections from normal and preeclamptic pregnant women were used. miR-203-induced inflammatory response was evaluated by the measurements of IL-6, IL-8, ICAM, and VCAM expression and production and neutrophil adhesion in the endothelial cells (EC) transfected with miR-203 precursor, pre-miR-203. SOCS3 expression was also determined. RESULTS: Up-regulation of miR-203 and ICAM expression and down-regulation of SOCS-3 expression were demonstrated in maternal vessel endothelium in preeclampsia. Overexpression of miR-203 resulted in down-regulation of SOCS-3 expression and increases in the production of IL-6, IL-8, ICAM, and VCAM and neutrophil adhesion in ECs. CONCLUSION: As miR-203 is an inflammatory microRNA, increased miR-203 production/expression in ECs could diminish an anti-inflammatory activity and increase the endothelial inflammatory response in preeclampsia.
PROBLEM: To determine whether miR-203 mediates endothelial inflammatory response in preeclampsia. METHOD OF STUDY: Maternal vessel miR-203 expression was assessed by in situ hybridization. Suppressor of cytokine signaling-3 (SOCS-3) and ICAM expression was determined by immunostaining. Subcutaneous fat tissue sections from normal and preeclamptic pregnant women were used. miR-203-induced inflammatory response was evaluated by the measurements of IL-6, IL-8, ICAM, and VCAM expression and production and neutrophil adhesion in the endothelial cells (EC) transfected with miR-203 precursor, pre-miR-203. SOCS3 expression was also determined. RESULTS: Up-regulation of miR-203 and ICAM expression and down-regulation of SOCS-3 expression were demonstrated in maternal vessel endothelium in preeclampsia. Overexpression of miR-203 resulted in down-regulation of SOCS-3 expression and increases in the production of IL-6, IL-8, ICAM, and VCAM and neutrophil adhesion in ECs. CONCLUSION: As miR-203 is an inflammatory microRNA, increased miR-203 production/expression in ECs could diminish an anti-inflammatory activity and increase the endothelial inflammatory response in preeclampsia.
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